By Gary Null, PhD, and Martin Feldman, MD
In Part 1 of this three-part series, we reviewed studies showing that the fluoridation of drinking water has not lived up to its promise in terms of reducing dental decay. We discussed the continuing support for water fluoridation from the U.S. government and the American Dental Association, but also presented the views of some former supporters of fluoridation who have begun to question the need for the process altogether. Finally, we examined the thin margin of safety that exists for fluoride and the multiple sources of fluoride exposure we face today.
In this second installment, we look at what occurs when a person’s fluoride intake exceeds the optimal level. The inescapable fact is that fluoride has been associated with severe health problems, ranging from dental fluorosis and skeletal fluorosis to bone fractures and even cancer.
According to a 1989 National Institute for Dental Research study, 1% to 2% of children living in areas fluoridated at 1 ppm develop dental fluorosis, or permanently stained, brown mottled teeth. Up to 23% of children living in areas naturally fluoridated at 4 ppm develop severe dental fluorosis.
In a 2000 study, researchers report that the prevalence of dental fluorosis in the United States has increased over the last 30 years in both fluoridated and nonfluoridated communities. They conclude that without intervention measures, such as using low-fluoride water to dilute infant formulas, supervising the toothbrushing of young children and changing fluoride supplement recommendations, the fluoride intakes of infants and children are likely to continue to increase and be associated with a further increase in the prevalence of enamel fluorosis.
The most critical period for fluoride exposure is the first year of life. A 1998 study reports that children exposed during this year, and to a lesser extent during the second year, are far more likely to develop fluorosis than those whose exposure begins later. The early mineralizing teeth—the central incisors and first molars—are the most likely to be affected. A study of rats suggests that dietary calcium helps protect teeth from fluoride toxicity to a certain extent. The level of dental fluorosis decreased with the increasing ingestion of calcium during the development of teeth.
A recent review of the literature identified four major risk factors for dental fluorosis. “There is substantial evidence that fluoridated water, fluoride supplements, infant formulas, and fluoride toothpastes are risk factors for fluorosis,” alone and together, reports Dr. Ana K. Mascarenhas of Ohio State University. And, too often, dentists and physicians misprescribe fluoride, she concludes. Two other studies indicate that African-American children may be at particular risk for dental fluorosis. One found higher levels of fluorosis in black children than in others studied; the other reported that an increase in dental fluorosis risk in several communities was greater among African-American children.
In “50 Reasons to Oppose Fluoridation,” Paul Connett, Ph.D., professor of chemistry at St. Lawrence University (N.Y.) who helped found the Fluoride Action Network (www.fluoridealert.org), observes that “the level of fluoride put into water (1 ppm) is 100 times higher than normally found in mothers’ milk (0.01 ppm). There are no benefits, only risks, for infants ingesting this heightened level of fluoride at such an early age (this is an age where susceptibility to environmental toxins is particularly high).”
Fluorosis gets worse as a child approaches puberty, according to study conducted in Norway. This study showed a significant increase in the severity of fluorosis with increasing age in a high fluoride community, whereas no change in severity with age was observed in a low fluoride community. Fluorosis resulting from high fluoride content of drinking water increases between the ages of 10 and 14.
Although the ADA and the government consider dental fluorosis only a cosmetic problem, the American Journal of Public Health says that “…brittleness of moderately and severely mottled teeth may be associated with elevated caries levels.” In these cases the fluoride is causing the exact problem it’s supposed to prevent. According to Dr. Yiamouyiannis, “In highly naturally-fluoridated areas, the teeth actually crumble as a result. These are the first visible symptoms of fluoride poisoning.”
In addition, the negative consequences of dental fluorosis go beyond the physical. The psychological effects of having moderately to severely mottled teeth also cannot be ignored. These effects were recognized in a 1984 National Institute of Mental Health panel that looked into this problem.
When fluoride is ingested, approximately 93% of it is absorbed into the bloodstream. A good part of this intake is excreted, but the rest is deposited in the bones and teeth and is capable of causing a crippling skeletal fluorosis.
Large numbers of people in Japan, China, India, the Middle East and Africa have been diagnosed with skeletal fluorosis from drinking naturally fluoridated water. In India alone, nearly a million people suffer from the affliction. While only a dozen cases of skeletal fluorosis have been reported in the United States, Chemical & Engineering News has stated that “critics of the EPA standard speculate that there probably have been many more cases of fluorosis—even crippling fluorosis—than the few reported in the literature because most doctors in the U.S. have not studied the disease and do not know how to diagnose it.” Because some symptoms of skeletal fluorosis mimic those of arthritis, the first two clinical phases of fluorosis can easily be misdiagnosed.
According to Dr. Connett, the causes of most forms of osteoarthritis are unknown. It is not implausible that the high prevalence of arthritis in America may be related to our high levels of fluoride intake. (Arthritis is one of the most prevalent diseases in the U.S.; nearly 43 million Americans have arthritis and related conditions.) A 2001 study in Turkey found that the severity of osteoarthritis of the knee was greater in patients with endemic fluorosis than in control subjects.
Radiologic changes in bone occur when fluoride exposure is 5 mg per day, according to the late Dr. Waldbott, author of Fluoridation: The Great Dilemma. While 5 mg per day level is the amount of fluoride ingested by most people living in fluoridated areas, the number increases for diabetics and laborers, who can ingest up to 20 mg of fluoride daily. In addition, a survey conducted by the Department of Agriculture shows that 3% of the U.S. population drinks 4 liters or more of water every day. If these individuals live in areas where the water contains a fluoride level of 4 ppm, allowed by the EPA, they are ingesting 16 mg per day from the consumption of water alone, and thus are at greater risk of developing skeletal fluorosis.
It bears mentioning that skeletal fluorosis may be associated with gastrointestinal problems. According to a study in India, all 10 patients with documented osteofluorosis experienced gastrointestinal symptoms, the most common being abdominal pain.
At one time, fluoride therapy was recommended to help build denser bones and prevent the fractures associated with osteoporosis. But several articles in peer-review journals suggest that fluoride actually does more harm than good because it is associated with bone breakage.
Three studies reported in the Journal of the American Medical Association showed links between hip fractures and fluoride., ,  A 1992 study, for example, found “a small but significant increase in the risk of hip fractures in both men and women exposed to artificial fluoridation at 1 ppm.” In addition, the New England Journal of Medicine has reported that people given fluoride to cure their osteoporosis actually end up with an increased nonvertebral fracture rate. Austrian researchers have also found that fluoride tablets make bones more susceptible to fractures.
Scientists at Yale University discovered that doses as low as 1 ppm of fluoride decrease bone strength and elasticity, making fracture more likely. Two studies published in the early 1990s found that the rate of hip fracture generally increased with exposure to fluoridated water, and the results of more recent studies have suggested that fluoride in water will increase the risk of hip fractures for certain age groups of women., 
Dr. Connett reports that of 18 studies conducted since 1990 on the possible link between fluoride and a greater rate of hip fractures in the elderly, 10 have found such an association. He states, “One study found a dose-related increase in hip fracture as the concentration of fluoride rose from 1 ppm to 8 ppm. Hip fracture is a very serious issue for the elderly, as a quarter of those who have a hip fracture die within a year of the operation, while 50 percent never regain an independent existence.” In 1989 the U.S. National Research Council reported that the U.S. hip fracture rate was the highest in the world.
One of the studies that did not find an association between exposure to fluoridated water and an increase in the risk of fracture was published in the British Medical Journal in 2000. The researchers reported no difference in the risk of humerus fracture and a non-significant trend toward an increased risk of wrist fracture. However, in a response to this study, Dr. Connett says that the “most disturbing aspect of the report is how much attention is given to the decrease of hip fracture incidence [deemed statistically significant] and how little attention is given to the increase in the incidence of wrist fracture [deemed statistically insignificant] in the group exposed for 20 years of water fluoridation.” The “significance” and “non-significance” of the change in fracture risks emerged only after adjustment for 12 variables, Dr. Connett explains. “It raises the question of how accurate these adjustments were, if such fine distinctions are going to be made.”
An editorial in Fluoride in 2000 describes the bone effects of fluoride in detail. Fluoride may increase bone quantity (osteofluorosis, osteosclerosis) but also decrease bone quality and bone strength. It is well known that pharmacological doses of fluoride increase the risk of torsion-type fractures (such as hip fractures) despite the appearance of greater bone density. Conventional medicine interprets the observed fluoride-induced increase of serum alkaline phosphatase concentration as a sign of osteoblast activity. Actually, it is a reflection of increased mortality of osteocytes within bone. Osteocytes are rich in alkaline phosphatase, which is released when the cells are killed by fluoride. It is therefore unlikely that a window of fluoride-induced bone benefit exists.
Fluoride’s deleterious effect on bone is well documented. Early experiments using large doses of fluoride as a treatment for osteoporosis had disastrous results. Dr. C. Rich warned that rather than strengthening bones, fluoride could cause osteoarthritis, as well as gastric pain, calcification of the arteries and visual disturbances. In 1980 a group of researchers found that fluoride accelerated the development of osteoporosis.
In an experiment on cow bone, fluoride treatment reduced the mechanical strength of bone tissue by converting small amounts of bone mineral to mostly calcium fluoride. This action reduces the structurally effective bone mineral content and possibly affects the interface bonding between the bone mineral and the organic matrix of the bone tissue. A Polish study published in 1999 found that treatment with fluoridated water decreases the bending strength of the femoral neck and shaft in laboratory rats.
When combined with a calcium deficiency, the effect of fluoride may be even worse. In a 2000 study of children in India, the toxic effects of fluoride were more complex and the incidence of metabolic bone disease and bony leg deformities was greater in calcium-deficient children than in those with adequate calcium.
A 1997 New Zealand review of scientific literature found a consistent pattern of evidence suggesting that fluoride damages bones; this evidence includes hip fractures, skeletal fluorosis, the effect of fluoride on bone structure, fluoride levels in bones and osteosarcomas. Public health authorities in Australia and New Zealand have appeared reluctant to consider openly and frankly the implications of this and earlier scientific evidence unfavorable to the continuing fluoridation of drinking water supplies.
Effects on the thyroid system
The supposedly safe fluoride levels in our water may pose a particular danger for any of the millions of people who suffer from thyroid disorders, reports Dr. Connett. He explains:
“Earlier in the 20th century, fluoride was prescribed by a number of European doctors to reduce the activity of the thyroid gland for those suffering from hyperthyroidism (overactive thyroid) (Merck Index, 1960, p. 952; Waldbott, et al., 1978, p. 163). With water fluoridation, we are forcing people to drink a thyroid-depressing medication which could serve to promote higher levels of hypothyroidism (underactive thyroid) in the population, and all the subsequent problems related to this disorder….
“It bears noting that according to the Department of Health and Human Services (1991) fluoride exposure in fluoridated communities is estimated to range from 1.58 to 6.6 mg/day, which is a range that actually overlaps the dose (2.3 – 4.5 mg/day) shown to decrease the functioning of the human thyroid (Goletti & Joyet, 1958). This is a remarkable fact, and certainly deserves greater attention considering the rampant and increasing problem of hypothyroidism in the United States. (In 1999, the second most prescribed drug of the year was Synthroid, which is a hormone replacement drug used to treat an underactive thyroid.)” More than 20 million people in the U.S. receive treatment for thyroid problems, and many others are thought to go undiagnosed. Keep in mind that 1 quart of water fluoridated at 1 ppm contains 1 milligram of fluoride.
Excess fluorine in drinking water was a risk factor for the more rapid development of thyroid pathology in a 1985 study. Water with a raised fluorine content resulted in several thyroid effects in healthy subjects, including an elevated production of thyroid stimulating hormone (TSH) and a decrease in the concentration of T3 hormone, compared with healthy people who drank water with a normal concentration of fluorine. An elevated level of TSH reflects an underactivity of the thyroid system. The pituitary gland releases TSH to direct the thyroid to manufacture thyroid hormone, but if the thyroid is sluggish in its response, then the pituitary will release excess TSH (hence, the elevated level) to try to further stimulate thyroid activity.
A 1996 study of 165 aluminum production workers with signs of chronic fluoride intoxication found thyroid abnormalities as well. They included a moderate reduction of the thyroid’s iodine-absorbing function, low T3 hormone with a normal level of T4 hormone, and a slight increase of TSH concentration.
A study of rats also found that fluoride caused a decrease in the levels of T3 and T4 hormones in plasma, a decrease in the free T4 index, and an increase in the T3-resin uptake ratio. In another study in which pregnant and lactating mice received fluoridated water, the pups had a 75% decrease in plasma free T4 at 14 days of age compared with a control group. A third study looked at the long-term effects of iodine and fluoride on the pathogenesis of goiters and fluorosis in mice. After 100 days of treatment, the fluoride showed some stimulatory effect on the thyroid in iodine-deficiency conditions and inhibitory effect in iodine-excess conditions.
Numerous studies demonstrate links between fluoridation and cancer. Toxicologist William Marcus has stated that “fluoride is a carcinogen by any standard we use. I believe EPA should act immediately to protect the public, not just on the cancer data, but on the evidence of bone fractures, arthritis, mutagenicity and other effects.”
A study published in the Journal of Epidemiology in 2001 found that about two-thirds of 36 cancer sites in the body were positively associated with fluoridated drinking water. The researchers examined the registered cancer rates for nine U.S. communities (with 21.8 million inhabitants) and used the percentage of people supplied with “optimally” fluoridated drinking water to perform a regression analysis of the incidence rates of cancers in the 36 sites. Of these, 23 were positively significant, nine were not significant, and four were negatively significant. Among the cancers positively associated with fluoridated drinking water were cancers of the oral cavity and pharynx, colon and rectum, hepato-biliary and urinary organs, as well as bone cancers in men, brain tumors and T-cell system Hodgkin’s disease, non-Hodgkin lymphoma, multiple myeloma, melanoma of the skin and monocytic leukemia.
Dr. Connett notes that “some of the earliest opponents of fluoride were biochemists and at least 14 Nobel prize winners are among numerous scientists who have expressed their reservations about the practice of fluoridation.” He cites Dr. James Sumner, winner of the Nobel Prize for his work on enzyme chemistry, who says, “We ought to go slowly. Everybody knows fluorine and fluoride are very poisonous substances…We use them in enzyme chemistry to poison enzymes, those vital agents in the body. That is the reason things are poisoned; because the enzymes are poisoned and that is why animals and plants die.”
Dr. Connett also cites two epidemiological studies suggesting a possible association between osteosarcoma (bone cancer) in young men and fluoridated areas. One is the report of the U.S. National Toxicology Program, which first uncovered the epidemiological evidence of increased osteosarcoma in boys and young men living in fluoridated areas. The second is a study conducted by the New Jersey Department of Health, in which Dr. Perry Cohn studied the incidence of the rare bone cancer in seven New Jersey counties relative to water fluoridation. In fluoridated areas, the incidence of osteosarcoma was 4.6 times higher than in unfluoridated areas in boys under the age of 10, 3.5 times higher in the 10 to 19 age group, and more than twice as high in the 20 to 49 age group.
A 2001 study of 20 osteosarcoma patients in India assessed the levels of fluoride in bone and explored the possible relationship with p53 mutations. The researchers propose that the “high fluoride bone content might have been one of the major factors causing osteosarcoma.”
Enzyme toxicity and genetic damage
Studies suggest that even a supposedly “safe” concentration of 1 ppm of fluoride added to drinking water can interfere with critical biological functions. This was demonstrated in 1977 at Austria’s Siebersdorf Research Center by Dr. W. Klein and colleagues, who found that even the low dose of 1 ppm inhibited DNA repair enzyme activity by 50% and caused genetic and chromosome damage.
A similar study conducted at the University of Missouri confirmed these results. In addition, scientists at Poland’s Pomeranian Medical Academy found that as little as 0.6 ppm of fluoride produced chromosomal damage to human white blood cells. And sperm cells displayed “a highly significant increase in mutation” after being treated with fluoride at Holland’s Leiden University.
When S.C. Freni participated in a 1991 U.S. Public Health Service review of the toxicity of fluoride, he searched for studies that correlated fluoride exposure with reproductive effects in humans. Freni discovered that in almost 50 years of fluoridation, no one had ever studied fluoride’s effect on the human fetus.
Several studies have since found that fluoride may have negative effects on the male reproductive system. In a 1996 study, researchers found that patients with skeletal fluorosis had significantly lower levels of circulating serum testosterones than did normal, healthy males living in areas nonendemic for fluorosis. (Other males who drank the same water as the fluorosis patients but had no clinical manifestations of the disease also had lower levels than the normal controls.) The decreased testosterone concentrations “suggest that fluoride toxicity may cause adverse effects in the reproductive system of males living in fluorosis endemic areas,” the researchers concluded. And in a 1994 study of mature rats treated with sodium fluoride, Narayana and Chinoy found that fluoride interferes with androgenesis and damages the testes by inhibiting the action of testosterone.
Several studies conducted in China link fluoride exposure to adverse effects on intelligence. In a 2000 study, researchers found that the IQ of 60 children aged 10 to 12 in a high-fluoride area was significantly lower than that of 58 children in a low-fluoride village. More children in the high-fluoride area (21.6%) were in the retardation or borderline IQ categories than their low-fluoride counterparts (3.4%). The researchers also found an inverse relationship between IQ and urinary fluoride level. They concluded: “Exposure of children to high levels of fluoride may therefore carry the risk of impaired development of intelligence.”
Another investigation measured the intelligence of children aged 8 to 13 living in areas with slight, medium and severe prevalence of fluorosis. It demonstrated a 15 to 19 point decrease in IQ among children in the fluorosis area compared with the nonfluorosis area. In addition, a 1994 study of children’s intelligence and the metabolism of iodine and fluorine revealed that exposure to high levels of fluoride increased the prevalence of thyroid enlargement (29.8%) and dental fluorosis (72.9%), while producing a slightly lower average IQ compared with control areas. The IQ differential was more pronounced (16.8%) when lower intelligence children were studied separately.
Dr. Connett cites a recent review by the Greater Boston Physicians for Social Responsibility which found that fluoride interferes with brain function in young animals and children.
Effect on the pineal gland
Another concern is fluoride’s effect on the pineal gland, a small but powerful structure located between the right and left hemispheres of the brain. The pineal gland secretes melatonin, a hormone that affects such functions as sleep cycles, jet lag, hybernation in animals, immunity and the onset of puberty.
Jennifer Luke, Ph.D., found that the pineal gland attracts fluoride and thereby interferes with the functions of melatonin. In autopsy studies, she discovered extremely high concentrations of fluoride in the gland, averaging 9,000 ppm and reaching 21,000 ppm in some cases. In an accompanying study of fluoride-treated Mongolian gerbils (the animal considered most favorable for studying effects on the pineal gland), Luke found lower levels of melatonin and earlier onset of puberty.
In addition, numerous studies have correlated insufficient melatonin production with an earlier-than-usual onset of puberty.,  A 1955 study in Newburgh and Kingston, N.Y., produced some extremely puzzling results that scientists have yet to explain. One was the finding that girls in fluoridated Newberg were reaching menstruation five months earlier on average than the girls in unfluoridated Kingston. This raises the question, does fluoride contribute to the alarming rates of early puberty that we are seeing? Premature menstruation is associated with a variety of ills, including breast cancer and obesity. A 2001 study published in the American Journal of Public Health reveals that early maturation nearly doubled the odds of being obese.
Elevated blood lead levels
Research conducted in recent years suggests that water fluoridation is associated with the harmful problem of increased blood levels of lead in children. Lead poisoning has been associated with higher rates of physical diseases and behavioral problems, and it has been a particular problem for African-American children, according to a report by Dr. Roger D. Masters, research professor of government and Nelson A. Rockefeller Professor Emeritus at Dartmouth College, and president of the Foundation for Neuroscience & Society.
Rogers and other researchers compared the blood lead levels of children living in communities whose water is treated with silicofluorides (SiFs), which serve more than 140 million Americans, with those in communities using sodium fluoride or with nonfluoridated water. In three samples that included more than 400,000 children in total, they found, “SiF-treated municipal water is always significantly associated with increased blood lead levels in children.”, , 
The research also found that this higher uptake of lead from the environment was especially pronounced among black children, who have higher blood levels of lead than do whites in similar environments. The research controlled for other risk factors associated with higher blood lead. But even when children living in communities with fewer risk factors for blood lead were compared with those in high-risk communities, the researchers found that “those exposed to silicofluoride-treated water are always worse off than those without these chemicals in their water, and these silicofluoride effects are worse when children are also exposed to many environmental risk factors for blood lead uptake. Moreover, these effects are strikingly worse for Black children than for whites.”
The greater uptake of lead is disturbing because high blood lead is associated with negative health and behavioral traits, including violent crime, cocaine use and asthma. When the researchers analyzed available data on these traits, they found that children exposed to SiF-treated water were more likely to have the behavioral or health problems that are more likely to occur among people with high levels of lead.
Rogers explains that lead poisoning disturbs the functioning of dopamine, a neurotransmitter that runs the brake pedal of the brain, among other actions. This neurotransmitter fires cells in areas of the brain that are associated with learning, impulse control, substance abuse and aggressive behavior. As a result, Rogers says, “lead increases the frequency of hyperactivity or learning disabilities, substance abuse and violent crime.” Because lead reduces impulse control, for example, children who have absorbed lead are more likely to grow up to have records of violent crime. Previous research shows that other toxic metals, such as manganese in abnormal levels, also can affect neurotransmitters and produce subtle behavioral effects. This research suggests that “traditional approaches to crime in the United States need to be reconsidered from an ecological point of view.”
As for the silicofluorides added to drinking water, Rogers points out that they have never been tested for safety. (All tests of water fluoridation were done with sodium fluoride.) He believes the U.S. should stop using SiFs until they have been fully tested by independent laboratories and proved to be safe. As it stands, he says, we are forcibly medicating people with a potentially dangerous and untested set of chemicals that compromise the lives of children.
His report concludes: “…It is hard to understand how responsible public health authorities could object to a moratorium on silicofluoride usage pending tests that demonstrate conclusively their safety. Our data indicate that such a step might well make a large contribution to reducing children’s blood lead levels and associated problems of health and behavior. Even more important, this action could have especially large benefits for thousands of Blacks living in poverty in many American cities.”
Fluoride and aluminum
Aluminum interacts with fluoride to create a toxic combination. A study conducted in Czechoslovakia adds force to the idea that aluminum may act synergistically with fluoride to trigger the mechanisms of Alzheimer’s disease. This study shows that some of the pathologic changes associated with AD are not induced by aluminum alone, but by the aluminofluoride complexes, which may act as the initial signal stimulating impairment of homeostasis, degeneration and death of the cells. By influencing energy metabolism, these complexes can accelerate the aging and impair the functions of the nervous system. “In respect to the etiology of AD, the long-term action of aluminofluoride complexes may represent a serious and powerful risk factor for the development of AD,” the authors conclude.
Incidentally, if you’re thinking that fluoride and aluminum are unlikely to come together in the normal course of things, think again. Fluoride is a direct byproduct of aluminum production. Aluminum is often added to drinking water as a flocculating agent by the same folks who add the fluoride—your local water authority.
Aluminum and fluoride form a number of complexes, the most deadly being aluminum tetrafluoride. Czech researchers have shown that the body reacts to aluminum tetrafluoride as if it were a phosphate ion capable of triggering G proteins. These are water-soluble substances (i.e., hormones, neurotransmitters and growth factors) that transmit messages from the outside to the inside of a cell. Aluminum tetrafluoride is capable of switching on G proteins without hormones, neurotransmitters or growth factors present.
Part 3 will cover fluoride accidents, how to avoid a fluoride overdose, one city’s rejection of fluoridation and the difficulties of challenging fluoridation.
Gary Null, PhD
P.O. Box 918
New York, New York 10024 USA
646-505-4660/ Fax 212-472-5139
Gary Null, PhD, has authored 50 books on health and nutrition and numerous articles published in leading magazines. Null holds a PhD in human nutrition and public health science from the Union Graduate School. He maintains a Web site at www.garynull.com that presents research articles on optimizing health through nutrition, lifestyle factors and alternative medicine.
Martin Feldman, MD, is assistant clinical professor of neurology at Mount Sinai Medical School in New York City. He practices complementary medicine.
 Fomon SJ, Ekstrand J, Ziegler EE. Fluoride intake and prevalence of dental fluorosis: trends in fluoride intake with special attention to infants. J Public Health Dent 2000 Summer; 60(3):131-9.
 Bardsen A, Bjorvatn K. Risk periods in the development of dental fluorosis. Clin Oral Investig 1998 Dec; 2(4):155-60.
 Ouyang W, Li Y, Liu Z, et al. Effect caused by uptake of different levels of calcium to enamel fluorosis in rats. (Article in Chinese) Zhonghua Kou Quiang Yi Xue Za Zhi 2000 Jan; 35(1):47-9.
 Mascarenhas, AK. Risk factors for dental fluorosis: a review of the recent literature. Pediatr Dent 2000 Jul-Aug; 22(4):269-77.
 Heller KE, Sohn W, Burt BA, Feigal RJ. Water consumption and nursing characteristics in infants by race and ethnicity. J Public Health Dent 2000 Summer; 60(3):140-6.
 Kumar JV, Swango PA. Fluoride exposure and dental fluorosis in Newburgh and Kingston, New York: policy implications. Community Dent Oral Epidemiol 1999 Jun; 27(3):171-80.
 Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board. National Academy Press, Washington DC, 1997. Cited in Connett P: 50 reasons to oppose fluoridation. Fluoride Action Network, at www.fluoridealert.org.
 Connett P. 50 reasons to oppose fluoridation. Fluoride Action Network, at www.fluoridealert.org.
 Rwenyonyi CM, Birkeland JM, Haugejorden O, Bjorvatn K. Age as a determinant of severity of dental fluorosis in children residing in areas with 0.5 and 2.5 mg fluoride per liter in drinking water. Clin Oral Investig 2000 Sep; 4(3):157-61.
 Butler WJ, Segreto V, Collins E. Prevalence of dental mottling in school-aged lifetime residents of 16 Texas communities. Am J Public Health 1985 Dec; 75(12):1408.
 Gary Null interview with Dr. John Yiamouyiannis, March 10, 1995.
 Grossman D. Fluoride’s revenge. The Progressive 1990 Dec; 29-31.
 Hileman B. Fluoridation of water. Chemical & Engineering News 1988 Aug 1; 66:49.
 Gary Null interview with Dr. John Yiamouyiannis, April 28, 1990.
 Hileman, op. cit., 36.
 Hileman, op. cit.
 Connett, op. cit.
 Arthritis: the nation’s leading cause of disability. National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA. Document last reviewed June 11, 2002. From www.cdc.gov/nccdphp/arthritis/index.htm.
 Savas S, Cetin M, Akdogan M, Heybeli N. Endemic fluorosis in Turkish patients: relationship with knee osteoarthritis. Rheumatol Int 2001 Sep; 21(1):30-5.
 Waldbott GL, Burgstahler AW, McKinney HL. Fluoridation: The Great Dilemma. Coronado Press Inc., Lawrence, KS, 1978, 38.
 Exner FB, Waldbott GL, Fluoride Poisoning in the Fluoridated Cities. Part II of The American Fluoridation Experiment. Edited by J Rorty. Devin-Adair Company, NY, 1957, 42-3.
 Dasarathy S, Das TK, Gupta IP, Susheela AK, Tandon RK. Gastroduodenal manifestations in patients with skeletal fluorosis. J Gastroenterol 1996 Jun; 31(3):333-7.
 Jacobsen SJ, Goldberg J, Miles TP, Brody JA, Stiers W, Rimm AA. Regional variation in the incidence of hip fracture: US white women aged 65 years and older. JAMA 1990 Jul 25; 264(4):500-2.
 Cooper C, Wickham CA, Barker DJ, Jacobsen SJ. Water fluoridation and hip fracture. JAMA 1991 Jul 24; 266:513-4. (Letter, a reanalysis of data presented in a 1990 paper.)
 Danielson C, Lyon JL, Egger M, Goodenough GK. Hip fractures and fluoridation in Utah’s elderly population. JAMA 1992 Aug 12; 268(6):746-8.
 Ibid, 746.
 Riggs BL, Hodson SF, O’Fallon WM, Chao EY, Wahner HW, et al. Effect of fluoride treatment on the fracture rates in postmenopausal women with osteoporosis. N Engl J Med 1990 Mar 22; 322(12):802-9.
 Hedlund LR, Gallagner JC. Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride. J Bone Miner Res 1989 Apr; 4(2):223-5.
 Albright JA. The effect of fluoride on the mechanical properties of bone. Transactions of the Annual Meeting of the Orthopedics Research Society. 1978; 40(15):1630-1.
 Gordon SL, Corbin SB. Summary of workshop on drinking water fluoride influence on hip fracture on bone health. (National Institutes of Health, 10 April, 1991) Osteoporos Int 1992 May: 2(3):109-17.
 Hegmann KT, Horne BD, Gren LH, Knight S, Orme HT, Lyon JL. The effects of fluoridation on degenerative joint disease (DJD) and hip fractures. Am J Epidemiol 2000 June Suppl Abstract 71.
 Kurttio P, Gustavsson N, Vartiainen T, Pekkanen J. Exposure to natural fluoride in well water and hip fracture: a cohort analysis in Finland. Am J Epidemiol 1999 Oct 15; 150(8):817-24.
 Connett, op. cit.
 Li Y, Liang C, Slemenda C, Ji R, Sun S, et al. Effect of long-term exposure to fluoride in drinking water on risks of bone fractures. J Bone Miner Res 2001 May; 16(5):932-9.
 Connett, op. cit.
 U.S. National Research Council. Diet and Health. National Academy Press, Washington DC, 1989, 121.
 Phipps KR, Orwoll ES, Mason JD, Cauley JA. Community water fluoridation, bone mineral density, and fractures: prospective study of effects in older women. BMJ 2000 Oct 7; 321(7265):860-4.
 Connett P, PhD. A response to Phipps’ study on hip fracture. International Fluoride Information Network (IFIN) Bulletin #156, 2000 Oct 11.
 Lee JR. Hip fractures and fluoride revisited: a critique. Editorial. Fluoride 2000 Feb; 33(1):1-5.
 Waldbott, op. cit., 81-4.
 Robin JC, Schepart B, Calkins H, LoSasso G, Thomas CC Jr, Ambrus JL. Studies on osteoporosis III. Effect of estrogens and fluoride. J Med 1980; 11(1):1-14.
 Kotha SP, Walsh WR, Pan Y, Guzelsu N. Varying the mechanical properties of bone tissue by changing the amount of its structurally effective bone mineral content. Biomed Mater Eng 1998; 8(5-6):321-34.
 Teotia M, Teotia SP, Singh KP. Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000. Indian J Pediatr 1998 May-Jun; 65(3):371-81.
 Colquhoun J. Why I changed my mind about water fluoridation. Perspect Biol Med 1997 Autumn; 41(1):29-44.
 Connett, op. cit., 50 reasons to oppose fluoridation.
 Galletti PM, Joyet G. Effect of fluorine on thyroidal iodine metabolism in hyperthyroidism. J Clin Endocrinol 1958 Oct; 18:1102-10.
 Ditkoff, Beth Ann and Lo Gerfo, Paul. The Thyroid Guide. Harper, New York, NY, 2000, cover notes.
 Bachinskii PP, Gutsalenko OA, Naryzhnuik ND, Sidora VD, Shliakhta AI. Action of the body fluorine of healthy persons and thyroidopathy patients on the function of hypophyseal-thyroid system. (Article in Russian) Probl Endokrinol (Mosk) 1985 Nov-Dec; 31(6):25-9.
 Mikhailets ND, Balabolkin MI, Rakitin VA, Danilov IP. Thyroid function during prolonged exposure to fluorides. Problemy Endokrinologii 1996; 42(1):6-9.
 Bobek S, Kahl S, Ewy Z. Effect of long-term fluoride administration on thyroid hormones level blood in rats. Endocrinol Exp 1976; 10(4):289-95.
 Trabelsi M, Guermazi F, Zeghal N. Effect of fluoride on thyroid function and cerebellar development in mice. Fluoride 2001; 34(3):165-73.
 Zhao W, Zhu H, Yu Z, Aoki K, Misumi J, Zhang X. Long-term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice. Endocr Regul 1998 Jun; 32(2):63-70.
 Griffiths, Joel. Fluoride: commie plot or capitalist ploy. Covert Action 1992 Fall; 42:66.
 Takahashi K, Akiniwa K, Narita K. Regression analysis of cancer incidence rates and water fluoride in the U.S.A. based on IACR/IARC (WHO) data (1978-1992). International Agency for Research on Cancer. J Epidemiol 2001 Jul; 11(4):170-79.
 Connett, op. cit., 50 reasons to oppose fluoridation.
 National Cancer Institute (1989). Cancer Statistics Review, 1973-1987, National Institutes of Health, Bethesda, MD, Publication No.90-2789.
 Cohn, PD. An Epidemiologic Report on Drinking Water and Fluoridation. 1992. New Jersey Department of Health, Trenton, NJ.
 Ramesh N, Vuayarahavan AS, Desai BS, Natarajan M, Murthy PB, Pillai KS. Low levels of p53 mutations in Indian patients with osteosarcoma and the correlation with fluoride levels in bone. J Environ Pathol Toxicol Oncol 2001; 20(3):237-43.
 Klein W et al. DNA repair and environmental substances. Zeitschrift fur Angewandte Bader-und Klimaheilkunde 1977; 24(3).
 Mohamed A, Chandler ME. Cytological effects of sodium fluoride on mice. Fluoride 1982 Jul; 15(3):110-18.
 Jachimczak D, Skotarczak B. The effect of fluorine and lead ions on the chromosomes of human leucocytes in vitro. Genetica Polonica 1978; 19(3):353-7.
 Mukherjee RN, Sobels FH. The effects of sodium fluoride and iodoacetamide on mutation induction by x-irradiation in mature spermatozoa of drosophila. Mutat Res 1968; 6:217-25.
 Cox WR. Hello Test Animals…Chinchillas or Your and Your Grandchildren. Milwaukee, WI: Olsen Publishing Co., 1951. Cited in Foulkes R. The fluoride connection: fluoride and the placental barrier. Townsend Letter for Doctors and Patients. Issue #177.
 Susheela AK, Jethanandani P. Circulating testosterone levels in skeletal fluorosis patients. J Toxicol Clin Toxicol 1996; 34(2):183-9.
 Narayana MV, Chinoy NJ. Effects of fluoride on rat testicular steroidogenesis. Fluoride 1994 Jan; 27(1):7-12.
 Lu Y, Sun ZR, Wu LN, Wang X, Lu W, Liu SS. Effect of high-fluoride water on intelligence in children. Fluoride 2000 May; 33(2):74-8.
 Li XS, Zhi JL, Gao, RQ. Effect of fluoride exposure on intelligence in children. Fluoride 1995; 28(4):189-92.
 Yang Y, Wang X, Guo X. Effects of high iodine and high fluorine on children’s intelligence and the metabolism of iodine and fluorine. Zhonghua Liu Xing Bing Xue Za Zhi 1994 Oct; 15(5):296-8.
 Shettler T, et al. In Harm’s Way: Toxic Threats to Child Development, Greater Boston Physicians for Social Responsibility, Cambridge, MA, May 2000.
 Luke J. Fluoride deposition in the aged human pineal gland. Caries Res 2001 Mar-Apr; 35(2):125-8.
 Luboshitzky R, Lavie P. Melatonin and sex hormone interrelationships—a review. J Pediatr Endocrinol Metab 1999 May-Jun; 12(3):355-62.
 Genazzani AR, Bernardi F, Monteleone P, Luisi S, Luisi M. Neuropeptides, neurotransmitters, neurosteroids, and the onset of puberty. Ann N Y Acad Sci 2000; 900:1-9.
 Okasha M, McCarron P, McEwen J, Smith GD. Age at menarche: secular trends and association with adult anthropometric measures. Ann Hum Biol 2001 Jan-Feb; 28(1):68-78.
 Adair LS, Gordon-Larsen P. Maturational timing and overweight prevalence in US adolescent girls. Am J Public Health 2001 Apr; 91(4):642-4.
 Masters RD. Silicofluorides and higher blood lead: a national problem that particularly harms blacks. Dartmouth College, Hanover, NH. Videoconference—Appalachian Environmental Lab, Frostburg State University, Frostburg, MD. November 15, 2001.
 Masters RD, Coplan MJ. Water treatment with silicofluorides and lead toxicity. Intern J Environ Studies 1999; 56:435-49.
 Masters RD, Coplan MJ, Hone BT, Dykes JE. Association of silicofluoride treated water with elevated blood lead. NeuroToxicology 2000; 21(6):1091-100.
 Masters RD, op. cit., Silicofluorides and higher blood lead: a national problem that particularly harms blacks.
 Gary Null interview with Dr. Roger Masters, July 24, 2002.
 Masters RD, op. cit., Silicofluorides and higher blood lead: a national problem that particularly harms blacks.
 Masters RD, Hone B, Doshi A. Environmental pollution, neurotoxicity and criminal violence. From Environmental Toxicology Current Developments. Environmental Topics, Vol. 7. J Rose, ed. Gordon and Breach Science Publishers, 1998, 26 & 37.
 Gary Null interview with Dr. Roger Masters, July 24, 2002.
 Masters RD, op. cit., Silicofluorides and higher blood lead: a national problem that particularly harms blacks.
 Strunecka A, Patocka J. Reassessment of the role of aluminum in the development of Alzheimer’s disease. Cesk Fysiol 1999 Feb; 48(1):9-15.
 Gary Null interview with Paul Connett, Ph.D., January 30, 2001.
 Strunecka A and Patocka J. Pharmacological and toxicological effects of aluminofluoride complexes. Fluoride 1999 Nov; 32(4):230-42.